EFFECT OF LOCAL TISSUE COOLING ON MICROVASCULAR SMOOTH-MUSCLE AND POSTJUNCTIONAL ALPHA-2-ADRENOCEPTORS
EFFECT OF LOCAL TISSUE COOLING ON MICROVASCULAR SMOOTH-MUSCLE AND POSTJUNCTIONAL ALPHA-2-ADRENOCEPTORS
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DOI:
10.1152/ajpheart.1988.255.1.h121
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发表时间:
1988-07-01
影响因子:
--
通讯作者:
FABER, JE
中科院分区:
文献类型:
--
作者:
FABER, JE
The effect of local tissue cooling on microvascular smooth muscle contractile behavior and sensitivity to adrenergic constriction was examined in rat cremaster skeletal muscle. Intravital microscopy was used to measure the diameter of first- and second-order arterioles (control diam=101 .+-. 7 .mu.m) and venules (diam=142 .+-. 9 .mu.m), and third-order terminal arterioles (diam=19 .+-. 4 .mu.m). Norepinephrine (NE) was added to the cremaster bath to produce a 20-35% reduction in control diameter obtained at 34.degree. C bath temperature (in situ cremaster temperature). In the presence of NE, cooling the bath to 26.degree. C caused additional constriction of large arterioles and venules. Terminal arterioles exhibited a more pronounced cooling-induced constriction. Spontaneous vasomotion, evident only in this vessel type, was abolished by cooling. Cooling-induced constriction and inhibition of vasomotion were readily reversible with rewarming to 34.degree. C. Blockade of postjunctional .alpha.2-adrenoceptors with yohimbine (1-5 .times. 10-7 M) completely abolished cooling-induced constriction, as did the .alpha.1- and .alpha.2-adrenoceptor antagonist phentolamine (10-6 M); blockade of .alpha.1-adrenoceptors with prazosin (10-8 M) had no effect on the response. After inhibition of the noradrenergic constriction with yohimbine or phentolamine, local cooling dilated terminal arterioles; however, the dilation was transient. These data suggest that modest tissue cooling has a direct, although transient, depressant effect on microvascular smooth muscle tone. However, in the presence of adrenergic constriction, the inhibitory effect of local tissue cooling is overcome by a selective increase in .alpha.2- but not .alpha.1-mediated vasoconstriction.